β-amyloid (Aβ) and copper play important roles in the pathogenesis of Alzheimer's disease (AD). However, the behavioral correlativity and molecular mechanisms of Aβ and copper toxicity have been investigated less often. In the present study, we investigated the interaction and toxicity of Aβ1-42 and copper in the Aβ1-42 transgenic Caenorhabditis elegans worm model CL2006. Our data show that the paralysis behavior of CL2006 worms significantly deteriorated after exposure to 10(-3) mol L(-1) copper ions. However, the paralysis behavior was dramatically attenuated with exposure to 10(-4) mol L(-1) copper ions. The exogenous copper treatment also partially changed the homeostatic balance of zinc, manganese, and iron. Our data suggest that the accumulation of reactive oxygen species (ROS) was responsible for the paralysis induced by Aβ and copper in CL2006. The ROS generation induced by Aβ and copper appear to be through sod-1, prdx-2, skn-1, hsp-60 and hsp-16.2 genes.